Critical Care

Shock

Circulatory failure types — hypovolemic, cardiogenic, distributive, obstructive

Shock is circulatory failure leading to inadequate tissue oxygen delivery and cellular dysfunction. Four major categories — hypovolemic (decreased preload from hemorrhage or fluid loss), cardiogenic (pump failure from MI, severe heart failure, arrhythmia), distributive (vasodilation from sepsis, anaphylaxis, neurogenic), and obstructive (mechanical impediment — tamponade, tension pneumothorax, massive PE). Common features: hypotension (MAP < 65 mmHg), tachycardia, oliguria, lactic acidosis, end-organ dysfunction. Hemodynamic profile differs by type: cold and clamped (low CO, high SVR) in hypovolemic/cardiogenic; warm and dilated (high CO, low SVR) in early septic. Treatment is type-specific but starts with airway, breathing, IV access, and fluids while diagnosing the cause. Mortality ranges 20-80% depending on type and timing.

  • Shock criteriaMAP < 65 mmHg + organ hypoperfusion
  • Lactate> 2 mmol/L (severe > 4)
  • HypovolemicHemorrhage; trauma, GI bleed, ruptured AAA
  • CardiogenicMI commonest; mortality 40-50%
  • Septic shockSepsis + vasopressors needed despite fluids
  • AnaphylaxisEpinephrine 0.3-0.5 mg IM (0.01 mg/kg)

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Why shock matters

  • Sepsis. Leading cause of in-hospital death; bundles save lives when delivered timely.
  • Trauma. Hemorrhagic shock is leading preventable cause of trauma death.
  • Cardiogenic shock. Post-MI complication with 40-50% mortality.
  • Anaphylaxis. Epinephrine within minutes is lifesaving — every minute matters.
  • Critical care. Every ICU admission requires shock differential and management plan.
  • Resuscitation. Code blue and rapid response systems built around shock recognition.
  • Surgery. Intraoperative shock requires immediate diagnosis (bleeding, anaphylaxis, cardiac).

Common misconceptions

  • Hypotension equals shock. Some shock has preserved BP (compensated); some hypotension is benign.
  • All shock needs fluids. Cardiogenic shock can worsen with fluids; consider type before bolus.
  • Lactate is just a marker. Lactate > 4 mmol/L is independent risk factor; trends matter.
  • Warm patient cannot be in shock. Distributive shock (sepsis, anaphylaxis) presents warm and flushed.
  • Anaphylaxis needs Benadryl first. Epinephrine is the priority; antihistamines are adjuncts.
  • Vasopressors fix everything. Need source control, fluid optimization, and treatment of underlying cause.

Frequently asked questions

How do the four shock types differ hemodynamically?

Hypovolemic: low preload (CVP/PCWP), low cardiac output, high SVR (compensatory vasoconstriction), cold extremities. Cardiogenic: high preload (PCWP > 18), low CO, high SVR, cold and clamped. Distributive: low SVR (vasodilation), often high CO (especially early sepsis), warm extremities, low diastolic pressure. Obstructive: variable preload depending on cause, low CO, high SVR. Pulmonary artery catheter or echocardiography distinguishes types when clinical exam is ambiguous. POCUS protocols (RUSH, FAST) are standard.

What is septic shock?

Sepsis (life-threatening organ dysfunction from dysregulated host response to infection) with persistent hypotension requiring vasopressors to maintain MAP ≥ 65 plus lactate > 2 despite adequate fluid resuscitation. Pathophysiology: inflammatory cytokines (TNF-α, IL-1, IL-6), nitric oxide-mediated vasodilation, capillary leak, microcirculatory dysfunction. Treatment bundle: blood cultures, broad-spectrum antibiotics within 1 hour, 30 mL/kg crystalloid bolus, norepinephrine first-line vasopressor (target MAP ≥ 65), source control, lactate clearance monitoring. Mortality 30-50%.

How is cardiogenic shock managed?

Most common cause is acute MI with > 40% LV damage. Diagnosis: hypotension, low CO (CI < 2.2), elevated PCWP > 18, signs of hypoperfusion. Treatment: emergent coronary revascularization (PCI within 90 min — DOOR-TO-BALLOON), inotropes (dobutamine, milrinone), vasopressors if MAP low (norepinephrine), mechanical support (IABP, Impella, ECMO/VA-ECMO) for refractory shock. Avoid excess fluids — exacerbates pulmonary edema. SHOCK trial showed early revascularization reduces mortality. Despite advances, mortality remains 40-50%.

What is anaphylaxis?

Severe systemic allergic reaction — IgE-mediated mast cell degranulation releases histamine, tryptase, leukotrienes. Clinical: urticaria, angioedema, bronchospasm, hypotension, GI symptoms. Common triggers: foods (peanut, shellfish, egg), drugs (penicillin, NSAIDs, anesthetics), insect stings, latex. Treatment: epinephrine 0.3-0.5 mg IM (0.01 mg/kg pediatric) — IM thigh fastest absorption, repeat every 5-15 min as needed. Adjuncts: airway, IV fluids, antihistamines (H1 + H2), steroids. Biphasic reactions in 5%. Discharge with EpiPen prescription and allergy referral.

How do you tell hemorrhagic shock class?

ATLS classification (70-kg adult): Class I (< 15%, < 750 mL): minimal symptoms. Class II (15-30%, 750-1500 mL): tachycardia, anxiety, narrowed pulse pressure. Class III (30-40%, 1500-2000 mL): hypotension, tachycardia > 120, confusion. Class IV (> 40%, > 2000 mL): severe hypotension, lethargy, oliguria, life-threatening. Treatment: damage-control resuscitation — permissive hypotension (SBP 80-90), 1:1:1 ratio of PRBCs:plasma:platelets, tranexamic acid within 3 hours (CRASH-2 trial), and rapid surgical control of bleeding source.

What about obstructive shock causes?

Tension pneumothorax: tracheal deviation, absent breath sounds, distended neck veins, hypotension. Treatment: needle decompression (2nd ICS midclavicular or 5th anterior axillary) then chest tube. Cardiac tamponade: Beck's triad (hypotension, JVD, muffled heart sounds), pulsus paradoxus, electrical alternans. Treatment: pericardiocentesis or surgical drainage. Massive PE: hypoxemia, RV strain, hemodynamic collapse. Treatment: thrombolysis (tPA 100 mg over 2 hours) or mechanical thrombectomy. All three are immediately reversible if recognized — high index of suspicion is life-saving.

How are vasopressors chosen?

Norepinephrine: first-line for septic and most distributive shock — α1 vasoconstriction, modest β1 inotropy. Epinephrine: α and β agonism, used for anaphylaxis, cardiogenic shock with bradycardia, severe sepsis when norepinephrine inadequate. Vasopressin: V1 receptor vasoconstriction, reduces norepinephrine requirement, useful in septic shock. Phenylephrine: pure α1 — used when tachycardia is problematic. Dobutamine: β1 inotrope for cardiogenic shock. Dopamine: dose-dependent (low: dopaminergic, mid: β, high: α) — fallen out of favor due to arrhythmogenic effects.